Bart Weijts

Abstract Tissue-resident macrophages populate nearly all organs, where they adopt tissue-specific roles essential for immune defense, tissue development and homeostasis. Their dysfunction contributes to inflammation, cancer and other diseases. Whether a dedicated macrophage population operates within the extensive vascular network, one of the body’s largest and most widely distributed tissues, has remained unknown.

Abstract De novo blood vessel formation occurs through coalescence of endothelial cells (ECs) into a cord-like structure, followed by lumenization either through cell-1,2,3 or cord-hollowing4,5,6,7. Vessels generated in this manner are restricted in diameter to one or two ECs, and these models fail to explain how vasculogenesis can form large-diameter vessels. Here, we describe a model for large vessel formation that does not require a cord-like structure or a hollowing step.

a complex biological process in which a tissue disruptor (pathogen or injury) is sensed, typically by immune cells, leading to the production of proinflammatory cytokines that activate the immune system to eliminate the cause of the disruption. In addition, tissue-resident cells and endothelial cells are activated to restore healthy tissue. lipids that act in the proximity of the producer cell to regulate inflammation.